Abstract
Transforming growth factor-β (TGF-β) is a crucial mediator in tissue fibrosis that promotes accumulation of extracellular matrix (ECM), myofibroblasts to epithelial–mesenchymal transition (EMT), endothelial-mesenchymal transition (EndoMT), and apoptosis via canonical and noncanonical signaling pathways. In the past decades, a number of microRNAs have been reported to participate in TGF-β-mediated tissue scarring; however, the roles of long noncoding RNAs (lncRNAs) in fibrogenesis remain largely unknown. Recently, emerging evidence has shown that lncRNAs are involved in the development of different diseases, including cancer, autoimmune diseases, cardiovascular diseases, and fibrotic diseases. In this review, we summarize the current updates of lncRNAs in TGF-β1-driven tissue fibrosis and discuss their therapeutic potential for the treatment of chronic fibrotic diseases.
Highlights
Tissue fibrosis is one of the main pathogenic mechanisms for end stage organ diseases that lead to high morbidity and increase health care burden worldwide [1]
Emerging evidence shows that noncoding RNAs, including microRNAs, short interfering RNAs, piwi-interacting RNAs, and various types of long ncRNAs [2] may be involved in the development and progression of fibrotic diseases [3,4]
Zhou et al identified over 3600 long ncRNAs (lncRNAs) that are expressed in human hepatic stellate cells (HSC) myofibroblasts
Summary
Tissue fibrosis is one of the main pathogenic mechanisms for end stage organ diseases (e.g., chronic kidney disease, liver cirrhosis, congestive heart failure) that lead to high morbidity and increase health care burden worldwide [1]. Understanding the underlying molecular mechanisms of tissue fibrosis would help to identify effective therapeutic targets for controlling chronic diseases. Emerging evidence shows that noncoding RNAs (ncRNAs), including microRNAs (miRNAs), short interfering RNAs (siRNAs), piwi-interacting RNAs (piRNAs), and various types of long ncRNAs (lncRNAs) [2] may be involved in the development and progression of fibrotic diseases [3,4]. The working mechanisms of miRNAs have been identified in many chronic diseases, including kidney disease, pulmonary fibrosis, and hepatic fibrosis [5,6]. Current findings regarding TGF-β1-driven fibrosis via lncRNAs and their therapeutic perspectives in organ fibrosis will be discussed in detail
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